Bim mediates mitochondria-regulated particulate matter-induced apoptosis in alveolar epithelial cells |
| |
Authors: | Zhang J Ghio A J Chang W Kamdar O Rosen G D Upadhyay D |
| |
Affiliation: | Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, 300 Pasteur Drive, Stanford, CA 94305-5236, USA. |
| |
Abstract: | We studied the role of Bim, a pro-apoptotic BCL-2 family member in Airborne particulate matter (PM 2.5 microm)-induced apoptosis in alveolar epithelial cells (AEC). PM induced AEC apoptosis by causing significant reduction of mitochondrial membrane potential and increase in caspase-9, caspase-3 and PARP-1 activation. PM upregulated pro-apoptotic protein Bim and enhanced translocation of Bim to the mitochondria. ShRNABim blocked PM-induced apoptosis by preventing activation of the mitochondrial death pathway suggesting a role of Bim in the regulation of mitochondrial pathway in AEC. Accordingly, we provide the evidence that Bim mediates PM-induced apoptosis via mitochondrial pathway. |
| |
Keywords: | AEC, alveolar epithelial cells Bim, pro-apoptotic BCL-2 family member PM, particulate matter ROS, reactive oxygen species |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|